Ethanol-induced neurological changes produce aversive withdrawal symptoms that often promote further ethanol abuse as a way of suppressing these unwanted conditions. Investigations designed to examine therapeutic interventions of ethanol withdrawal are clinically relevant in that they may result in a reduction in the probability of further abuse [unreadable] episodes. Although most alcohol research, to date, has focused primarily upon ethanol-induced disruptions in neurotransmitter homeostasis, changes in the neuroendocrine control of systemic osmolarity also appear to exist as a contributing factor of withdrawal severity. However, the p-amino acid taurine, with recognized functions in osmoregulation and neuroinhibition via GABA and glycine receptors, might ameliorate these ethanol-provoked alterations and reduce overall withdrawal severity. The proposed investigation will examine the possible therapeutic effect of taurine in alleviating ethanol withdrawal as determined by measures of withdrawal-related handling-induced convulsions. The design of the experiments will allow the dissociation of taurine's action via osmoregulation and/or neuroinhibition in male C3H mice made ethanol dependent through chronic exposure to ethanol vapors. In addition, levels of arginine vasopressin, taurine, and GABA will be measured in the highly osmosensitive supraoptic nucleus of the hypothalamus, pituitary, and hippocampus. Results from these studies could provide evidence that supports the therapeutic use of taurine in alcoholism and lead to further investigations of the therapeutic use of this amino acid. [unreadable] [unreadable]